01Approach to the Critical Patient/attcp49

Tamponade recognition and immediate action

›Hemodynamic threat identification

›Beck's triad: hypotension, elevated JVP, muffled heart sounds

›Classic triad present in minority of tamponade cases

›Absence does not exclude tamponade

›Pulsus paradoxus >10 mmHg inspiratory drop in systolic BP

›Most specific clinical sign of tamponade physiology

›Measure with manual sphygmomanometer during quiet breathing

›Tachycardia as earliest and most sensitive compensatory sign

›Absent in patients on beta-blockers or with hypothyroidism

›If hemodynamic collapse, immediate pericardiocentesis or surgical drainage

›Class I recommendation

›Do not delay for echocardiographic confirmation in extremis

Stabilization priorities

›Airway and oxygenation

›Supplemental oxygen to SpO2 >92%

›Dyspnea present in 65.9% of pericardial effusions

›Orthopnea without pulmonary rales distinguishes tamponade from CHF

›Avoid positive-pressure ventilation when tamponade suspected

›PPV reduces venous return and can precipitate cardiovascular collapse

›Use only when airway protection is absolutely required

›Circulatory support

›IV access: two large-bore peripheral lines

›IV fluid challenge 500 mL normal saline to maintain preload

›Avoid diuretics and vasodilators — can precipitate collapse

›Vasopressors if fluid fails: norepinephrine preferred

›Dopamine as alternative if norepinephrine unavailable

›Avoid IV sedation unless absolutely necessary

02History/hx63

Presenting symptoms

›Dyspnea

›Most common presenting symptom overall: 65.9% of pericardial effusions

›Orthopnea suggests significant effusion size

›Rapid worsening over hours suggests acute accumulation

›Chest pain

›Sharp, pleuritic, positional character

›Worse supine, improved by sitting forward

›Present in ~90% of pericarditis-associated effusions

›Radiation to trapezius ridge: phrenic nerve irritation by pericardial inflammation

›Constitutional symptoms

›Low-grade fever: inflammatory or infectious etiology

›Weight loss and night sweats: malignancy or tuberculosis

›Fatigue and palpitations

›Syncope or presyncope

›Suggests significant hemodynamic compromise

›Tamponade or large effusion with impaired cardiac output

Onset and temporal features

›Time course classification

›Acute onset: hours to days — infectious, traumatic, post-procedure

›Subacute: days to weeks — inflammatory, autoimmune, early malignancy

›Chronic: >3 months — malignancy, TB, hypothyroidism, uremia

›Rapidity of progression

›Rapid accumulation causes tamponade at lower volumes than gradual

›Acute 150–200 mL can cause tamponade

›Chronic effusions can exceed 2 L without tamponade

Triggers and exposures

›Recent viral illness

03Physical Exam/exam42

Vital signs

›Hemodynamic stability assessment

›Heart rate

›Tachycardia: most sensitive clinical sign of tamponade

›Rate >100 bpm in absence of fever raises concern

›Blood pressure

›Hypotension: late finding; may be absent early due to compensation

›SBP <90 mmHg or MAP <65 mmHg: hemodynamic compromise

›Pulsus paradoxus measurement

›>10 mmHg inspiratory drop in systolic BP: most specific tamponade sign

›Absent in atrial septal defect, severe aortic regurgitation, positive-pressure ventilation

›Respiratory rate

›Tachypnea from dyspnea or reduced cardiac output

Cardiovascular exam

›Cardiac auscultation

›Muffled or distant heart sounds

›Present with large effusion; absent with small effusion

›Pericardial friction rub

›High-pitched, triphasic, scratchy sound

›Best heard leaning forward at end-expiration

›Present in <30% of pericarditis-associated effusions

›Usually absent with large effusions

›Jugular venous pressure

›Elevated JVP with tamponade physiology

›Kussmaul sign (JVP rising with inspiration): suggests constrictive physiology

›Absent in hypovolemia-associated tamponade

›Peripheral perfusion

›Cool extremities: low cardiac output state

04Differential Diagnosis/ddx43

Life-threatening diagnoses

›Cardiac tamponade

›ICD-10: I31.9 (pericardial effusion, unspecified)

›Rapid accumulation causing hemodynamic compromise

›Cannot-miss: echocardiogram immediately

›Aortic dissection with hemopericardium

›ICD-10: I71.0x

›Sudden onset tearing chest pain, pulse deficits

›Requires emergent surgical management; pericardiocentesis contraindicated

›Myocardial rupture post-MI

›ICD-10: I23.3

›Acute hemopericardium; catastrophic presentation

Inflammatory and infectious causes

›Acute pericarditis with effusion

›ICD-10: I30.9

›Pleuritic chest pain, friction rub, ST elevation on ECG

›Viral pericarditis most common in North America

›Purulent (bacterial) pericarditis

›ICD-10: I30.1

›High fever, toxic appearance, rapidly accumulating effusion

›Tuberculous pericarditis

›ICD-10: A18.84

›Subacute onset, constitutional symptoms, endemic risk factors

Autoimmune and malignant causes

›Malignant pericardial effusion

›ICD-10: C45.2 (mesothelioma) or C79.89 (secondary)

›Often large, recurrent; cytology positive in ~75%

›Lupus pericarditis

05Laboratory Tests/lt49

Core inflammatory and infection markers

›C-reactive protein and ESR

›CRP elevated in ~78% of inflammatory pericarditis

›Guides treatment response and recurrence monitoring

›Normalization supports safe discontinuation of anti-inflammatory therapy

›ESR elevated in most inflammatory etiologies

›Less specific than CRP for monitoring

›Complete blood count with differential

›Neutrophilic leukocytosis: inflammatory or bacterial etiology

›Elevated neutrophil-to-lymphocyte ratio: inflammatory marker

›Lymphocytosis: viral or TB etiology consideration

›Troponin

›Evaluate for myopericarditis

›Elevated in ~15% of pericarditis cases

›Elevation not a negative prognostic marker if LV function preserved

›Serial troponin if myocarditis suspected

Metabolic and organ function

›Basic metabolic panel and renal function

›Uremia: BUN and creatinine elevation

›Uremic pericarditis present in 25% of some ESRD series

›Electrolytes: sodium, potassium for management planning

›Thyroid-stimulating hormone

›Hypothyroidism: myxedema pericardial effusion

›TSH elevation can present with large chronic effusion

›Thyroid replacement resolves effusion in most cases

›Liver function tests

›Hepatic disease as cause of transudative effusion

›Relevant for drug metabolism in treatment planning

06Diagnostic Tests/dt99

Scoring Systems

›Mayo Clinic risk stratification tool for pericarditis

›High-risk features predicting complicated course

›Temperature >38°C

›Subacute onset without clear trigger

›Large effusion >2.0 cm on echocardiography

›Failure to respond to NSAID therapy within 1 week

›Troponin elevation with LV dysfunction

›High-risk features indicating hospital admission

›One or more high-risk feature warrants admission per ACC 2025 guidance

›CARDIAC TAMPONADE clinical scoring

›Hemodynamic criteria

›Pulsus paradoxus >10 mmHg

›Hypotension: SBP <90 mmHg

›Tachycardia >100 bpm

›Echocardiographic criteria (Spodick criteria)

›Right atrial collapse lasting >1/3 of cardiac cycle

›Right ventricular diastolic collapse

›IVC plethora without inspiratory collapse

›Respirophasic variation >25% in mitral, >40% in tricuspid flow velocities

MRI

›Cardiac MRI indications and capabilities

›Preferred modality for pericardial tissue characterization

›Pericardial thickness assessment: normal <2 mm

›Pericardial enhancement on late gadolinium: active inflammation

›Effusion characterization

›T1 signal: hemorrhagic vs. serous effusion

›T2 signal: inflammatory activity

›Myocarditis evaluation

›Lake Louise criteria for myopericarditis

›LGE pattern to differentiate ischemic from non-ischemic

›Constrictive pericarditis assessment

›Real-time cine MRI: septal bounce with respiration

›Pericardial calcification complementary to CT

›Limitations

›Not for acute unstable patients

›Contraindicated in non-MRI-compatible devices

›Limited availability and time requirements

CT

›CT chest indications

›Pericardial effusion characterization

›Effusion attenuation values: serous (0–30 HU), hemorrhagic (>50 HU), exudative (>50 HU)

›Pericardial thickening >4 mm: suggests constrictive or inflammatory disease

›Aortic dissection evaluation

›CT angiography chest: first-line for dissection with hemopericardium

›Sensitivity approaching 100%, specificity approaching 100%

›Type A dissection with hemopericardium: surgical emergency

›Malignancy staging

›Mediastinal lymphadenopathy, pulmonary masses, pleural involvement

›Integral to staging workup for suspected malignant effusion

›Pericardial calcification

›Best seen on non-contrast CT

›Eggshell calcification in chronic constrictive pericarditis

›Post-procedure effusion assessment

›Loculated effusion identification for drainage planning

Ultrasound

›Point-of-care ultrasound (POCUS) first-line

›Sensitivity and specificity

›Sensitivity >95% for pericardial effusion detection

›Echocardiography is gold standard for tamponade diagnosis

›Effusion grading by echo-free space

›Small: <0.5 cm

›Moderate: 0.5–2.0 cm

›Large: >2.0 cm

›Tamponade features on echocardiography

›RA free wall collapse: earliest sign, present in most tamponade

›RV diastolic collapse: more specific for tamponade

›IVC plethora: dilated IVC >2.1 cm without inspiratory collapse

›Respirophasic mitral E-wave variation >25%: equivalent to pulsus paradoxus

›Pleural effusion differentiation

›Parasternal long-axis view: pericardial effusion anterior to descending aorta

›Pleural effusion posterior to descending aorta

›Epicardial fat pad differentiation

›Echodense, moves synchronously with myocardium

›Pericardial effusion: anechoic, does not move with myocardium

›Pericardiocentesis guidance

›POCUS-guided approach preferred: safer than blind technique

›Subxiphoid or apical approach based on effusion distribution

›Formal transthoracic echocardiography (TTE)

›Serial TTE to monitor effusion size and cardiac function

›Repeat TTE within 1 week for moderate-to-large effusions

ECG findings

›ECG interpretation in pericardial effusion

›Electrical alternans

›Alternating QRS axis beat-to-beat: heart swinging in effusion

›Highly specific for large effusion with cardiac tamponade

›Sensitivity limited: present in large effusions only

›Low QRS voltage

›QRS amplitude <5 mm in limb leads or <10 mm in precordial leads

›Seen in moderate-to-large effusions

›Reversible after pericardiocentesis

›Diffuse ST elevation

›Saddle-shaped ST elevation without reciprocal depression in pericarditis

›PR depression in multiple leads: early and specific pericarditis sign

›Sinus tachycardia

›Most common ECG finding in tamponade

Chest X-ray

›CXR findings

›Cardiomegaly

›Water bottle or flask-shaped cardiac silhouette

›Sensitivity low for small effusions

›Pulmonary vascularity

›Normal pulmonary vascularity distinguishes pericardial effusion from pulmonary edema

›Pleural effusions

›Concurrent in many inflammatory and malignant etiologies

07Disposition/dispo35

Admission indications

›Criteria requiring inpatient admission

›Cardiac tamponade or hemodynamic compromise

›ICU-level monitoring mandatory

›Pericardiocentesis team activation

›Large pericardial effusion >2.0 cm on echocardiography with any symptoms

›High fever >38°C: concern for purulent pericarditis or systemic infection

›Subacute onset without clear trigger

›Concern for malignancy or tuberculosis

›Failure to respond to prior NSAID therapy

›Suspected bacterial or malignant etiology

›Myopericarditis with LV dysfunction

›Need for diagnostic or therapeutic pericardiocentesis

Discharge criteria

›Criteria permitting discharge

›Small-to-moderate effusion without hemodynamic compromise

›Pulsus paradoxus <10 mmHg

›No tachycardia or hypotension

›Known etiology with appropriate outpatient treatment plan

›Hemodynamically stable with pain controlled on oral anti-inflammatories

›Reliable follow-up arranged

›Cardiology follow-up within 1–2 weeks

›Repeat echocardiography within 1 week for moderate effusions

Transfer and consultation criteria

›Transfer triggers

›Cardiac tamponade requiring pericardiocentesis beyond facility capability

›Hemopericardium from aortic dissection: emergent cardiothoracic surgery transfer

›Loculated or malignant effusion requiring surgical pericardial window

08Treatment/t74

Emergency management of cardiac tamponade

›Pericardiocentesis

›Indications

›Cardiac tamponade with hemodynamic compromise: Class I recommendation

›Suspected bacterial, TB, or malignant etiology for diagnosis

›Not recommended for effusion without tamponade physiology

›Technique

›POCUS-guided approach preferred over blind technique

›Subxiphoid approach: needle aimed 45 degrees toward left shoulder

›Apical approach: alternative based on effusion location

›Aspiration of small volume (20–50 mL) can rapidly restore hemodynamics

›Post-procedure management

›Drain placement for 3–5 days if ongoing drainage needed

›Surgical pericardial window if high output persists at 6–7 days

›Post-pericardiocentesis TTE to assess residual effusion and cardiac function

›Contraindications

›Hemopericardium from aortic dissection: pericardiocentesis releases tamponade, enabling dissection propagation

›Coagulopathy: correct prior to elective procedure

Anti-inflammatory treatment — inflammatory pericarditis

›First-line therapy

›Ibuprofen

›Dose: 600–800 mg orally every 8 hours

›Duration: 2–4 weeks for acute episode

›Taper over 2–4 weeks once symptom-free and CRP normalized

›Alternative: aspirin 650–1000 mg every 6–8 hours

›Colchicine

›Dose: 0.5 mg twice daily (weight >70 kg) or 0.5 mg once daily (weight <70 kg)

›Duration: 3 months for acute episode

›Duration: 6 months or longer for recurrent pericarditis

›Evidence base: COPE and ICAP trials showing 50% reduction in recurrence

›Do not discontinue early: early cessation increases recurrence risk

›Gastroprotection

›PPI recommended with high-dose NSAIDs

›Corticosteroids

›Reserved for NSAID and colchicine failure

›Prednisone 0.25–0.5 mg/kg/day

›Higher doses increase recurrence risk

›Taper slowly: reduce by 25–50% per week once CRP normalizes

›Avoid corticosteroids in first-line treatment

›Associated with higher rates of recurrence and chronicity

Refractory inflammatory pericarditis

›Anti-IL-1 agents

›Anakinra

›Dose: 100 mg subcutaneously daily

›Indicated for colchicine-resistant recurrent pericarditis

›Evidence: AIRTRIP trial

›Rilonacept

›Dose: 320 mg subcutaneous loading, then 160 mg weekly

›FDA-approved for recurrent pericarditis

›Evidence: RHAPSODY trial showing significant reduction in recurrence

›IVIG

›Alternative in refractory cases not responding to IL-1 blockade

Non-inflammatory effusion management

›Treat underlying cause

›Uremic pericardial effusion

›Intensify dialysis: most cases resolve with adequate dialysis

›NSAIDs not first-line; dialysis is preferred

›Hypothyroid effusion

›Thyroid hormone replacement: levothyroxine titrated to normalize TSH

›Effusion resolves with euthyroid state

›Malignant effusion

›Systemic oncologic therapy directed at underlying malignancy

›Sclerosing agents post-pericardiocentesis to prevent recurrence

›Pericardial window for recurrent malignant effusions

›Serial monitoring for small stable effusions

›Surveillance TTE for small-to-moderate asymptomatic effusions

›Exercise restriction not required in absence of pericardial inflammation

Post-MI pericarditis treatment

›Dressler syndrome

›Aspirin preferred: 650 mg every 6–8 hours

›Avoid other NSAIDs: risk of impaired myocardial healing

›Avoid corticosteroids in early post-MI period

›Risk of impaired infarct healing and myocardial rupture

›Colchicine can be added per ACC 2025 guidance

Activity restriction

›Exercise restriction in inflammatory pericarditis

›Avoid strenuous exercise for minimum 1 month

›Maximum heart rate target <100 bpm during restriction period

›Athletes: return to sport after symptom resolution and CRP normalization

›Evidence level: Class I recommendation for competitive athletes

09Special Populations/sp59

Pregnancy

›Physiologic considerations

›Increased blood volume and cardiac output alter hemodynamic assessment

›Pulsus paradoxus interpretation requires pregnancy-adjusted norms

›Tachycardia physiologic in pregnancy complicates tamponade assessment

›Physiologic pericardial effusion common in third trimester

›Small effusion in late pregnancy usually benign and resolves postpartum

›Medication safety

›NSAID restrictions

›Ibuprofen and aspirin: avoid after 20 weeks gestation

›Risk of premature closure of ductus arteriosus

›Low-dose aspirin (81 mg) may be continued for other indications

›Colchicine in pregnancy

›Limited safety data; generally avoided

›Consult rheumatology and maternal-fetal medicine

›Corticosteroids

›Prednisone: preferred if systemic anti-inflammatory required in pregnancy

›Risk-benefit assessment with obstetrics team

›Pericardiocentesis in pregnancy

›Tamponade: pericardiocentesis indicated regardless of gestational age

›POCUS guidance preferred to minimize fetal radiation

›Multidisciplinary team: cardiology, obstetrics, anesthesia

Geriatric

›Epidemiology differences

›Malignancy more common cause in elderly patients

›Atrial fibrillation may mask tachycardia as tamponade sign

›Chronic effusions more prevalent; natural history data limited

›Clinical presentation differences

10Background/b69

Epidemiology

›Prevalence and incidence

›Pericardial effusion detected in 3–5% of unselected echocardiograms

›Prevalence increases with cancer, renal failure, and immunosuppression

›Tamponade incidence: approximately 2 per 10,000 hospitalizations in Western populations

›Etiologic distribution in North America and Western Europe

›Idiopathic or viral: ~50% of all cases

›Malignancy-related: 13–23% of cases

›Post-cardiac surgery and procedural: 15–20% of cases

›Autoimmune: 5–10% of cases

›Bacterial: <5% in Western countries

›Etiologic distribution globally

›TB pericarditis: predominant cause in endemic regions (Sub-Saharan Africa, Southeast Asia)

›TB accounts for 60–80% of pericardial effusion in HIV-endemic settings

›Outcomes

›In-hospital mortality for cardiac tamponade requiring pericardiocentesis: 3–5% in high-resource settings

›Recurrence rate after first pericarditis episode: 15–30%

›Large chronic asymptomatic effusions: up to one-third may progress to tamponade

Pathophysiology

›Pericardial space anatomy

›Normal pericardial fluid volume: 15–50 mL

›Pericardium consists of fibrous outer layer and serous inner layer

›Pericardial compliance determines hemodynamic impact of effusion

›Volume-pressure relationship

›Acute accumulation: steep pressure-volume curve

›Small acute volumes (150–200 mL) can cause tamponade

›Chronic accumulation: pericardium stretches; gradual compliance increase

›Large chronic volumes (>2 L) can accumulate without tamponade

›Tamponade physiology

›Rising intrapericardial pressure compresses cardiac chambers

›Sequential chamber compression: RA collapses first, then RV in diastole

›Reduced ventricular filling: stroke volume falls, compensatory tachycardia

›Respiratory variation: inspiratory RV filling increases at expense of LV

›Mechanism of pulsus paradoxus: exaggerated septal shift

›Decompensation: BP falls when compensatory mechanisms exhausted

›Effusion classification by size

›Small: <0.5 cm echo-free space

›Moderate: 0.5–2.0 cm echo-free space

›Large: >2.0 cm echo-free space

›Effusion type by composition

›Serous: transudative causes (CHF, hypoalbuminemia)

›Serosanguineous or hemorrhagic: malignancy, trauma, anticoagulation

›Exudative: inflammatory, infectious, autoimmune

›Chylous: lymphatic obstruction (rare)

Therapeutic Considerations

›Anti-inflammatory therapy rationale

›NSAIDs: COX inhibition reduces prostaglandin-mediated inflammation

›First-line for pericarditis-associated effusion

›Aspirin preferred in post-MI pericarditis to avoid MI healing impairment

›Colchicine: inhibits microtubule polymerization and neutrophil migration

›Additive to NSAID therapy; reduces recurrence by 50% in COPE and ICAP trials

›Duration at least 3 months for acute, 6+ months for recurrent

›Corticosteroids: broad immunosuppression

›Reserved for refractory cases; associated with higher recurrence rates

›IL-1 inhibitors: target upstream inflammatory pathway

›Anakinra and rilonacept: evidence-based for refractory recurrent pericarditis

›Pericardiocentesis technique considerations

›Echocardiographic guidance preferred

›Reduces complication rate compared to blind technique

›Real-time needle visualization preferred over static guidance

›Contrast injection through needle verifies pericardial vs. ventricular position

›Post-drainage drain placement reduces recurrence

›Surgical options

›Pericardial window: for recurrent or malignant effusions

›Subxiphoid approach: preferred for frail or high-risk patients

›Video-assisted thoracoscopic (VATS) pericardiectomy: alternative

›Pericardiectomy: for constrictive pericarditis

›Monitoring strategy

›CRP normalization as treatment endpoint

›Guides duration and discontinuation of anti-inflammatory therapy

›Serial echocardiography for effusion size tracking

›Repeat within 1 week for moderate-to-large effusions

11Patient Discharge Instructions/pdi35

copy discharge instructions

›Diagnosis and what it means

›Pericardial effusion: fluid collected around your heart

›Can be caused by infection, inflammation, autoimmune disease, or other conditions

›Most small-to-moderate effusions improve with medication and time

›Medications at home

›Take your anti-inflammatory medication exactly as prescribed

›Ibuprofen or aspirin: take with food to reduce stomach irritation

›Do not stop early even if you feel better

›Colchicine: take every day for the full prescribed course

›Stopping early greatly increases the chance of your effusion and inflammation returning

›Take the stomach-protecting medication (PPI) with your anti-inflammatory

›Activity restrictions

›No strenuous physical activity, heavy lifting, or vigorous exercise for at least 1 month

›Keep your heart rate below 100 beats per minute during this period

›Light walking is acceptable

›No competitive sports until cleared by your cardiologist

›Follow-up appointments

›Cardiology follow-up within 1–2 weeks of discharge

›Repeat echocardiogram (heart ultrasound) within 1 week as arranged

›Blood test (CRP) monitoring to ensure inflammation is resolving

›Return to emergency department immediately if

›Worsening shortness of breath or new inability to lie flat

›Lightheadedness, dizziness, or fainting

›Worsening chest pain

›Rapid or irregular heart rate

›Swelling in legs or abdomen

›New fever or chills

12References/r30

Guidelines and key sources

›ACC 2025 Expert Consensus Statement on Pericarditis

›Wang TKM, Klein AL, Cremer PC, et al. 2025 Concise Clinical Guidance: ACC Expert Consensus Statement on the Diagnosis and Management of Pericarditis. Journal of the American College of Cardiology. 2025

›Primary evidence source for risk stratification, treatment algorithms, and colchicine duration

›JAMA Review 2024

›Cremer PC, Klein AL, Imazio M. Diagnosis, Risk Stratification, and Treatment of Pericarditis: A Review. JAMA. 2024

›Key epidemiologic statistics and treatment evidence synthesis

›JACC Cardiovascular Imaging 2024

›Klein AL, Wang TKM, Cremer PC, et al. Pericardial Diseases: International Position Statement on New Concepts and Advances in Multimodality Cardiac Imaging. JACC Cardiovascular Imaging. 2024

›Multimodality imaging protocols for echocardiography, CT, and MRI

Landmark trials

›COPE Trial

›Imazio M, et al. Colchicine for Recurrent Pericarditis. Circulation. 2005

›Colchicine reduced recurrence by 50% in first acute episode

›ICAP Trial

›Imazio M, et al. A Randomized Trial of Colchicine for Acute Pericarditis. NEJM. 2013

›Confirmed colchicine benefit as adjunct to aspirin: NNT 8 to prevent one recurrence

›AIRTRIP Trial

›Imazio M, et al. Anakinra for Corticosteroid-Dependent and Colchicine-Resistant Pericarditis. Heart. 2016

›Anakinra reduced recurrence in refractory inflammatory pericarditis

›RHAPSODY Trial

›Klein AL, et al. Phase 3 Trial of Interleukin-1 Trap Rilonacept in Recurrent Pericarditis. NEJM. 2021

›Rilonacept reduced recurrence by 96% vs. placebo; FDA approval basis

Additional references

›Cardiac tamponade review

›Adler Y, Ristic AD, Imazio M, et al. Cardiac Tamponade. Nature Reviews Disease Primers. 2023

›Spodick DH. Acute Cardiac Tamponade. NEJM. 2003

›Chronic pericardial effusion management

Evidence & Review

Evidence & Review